Urinary compounds in autism.

BACKGROUND: Although earlier claims to identify specific compounds in the urine of people with autism had been discredited, it was subsequently suggested that there might be biochemical characteristics that were specific to early childhood, particularly in those who also did not have a severe degree of intellectual disability This study was to establish whether autism might have a distinctive chromatographic profile on urinary analysis. METHOD: Thirty-four prepubertal boys with autism were matched with two groups of boys without autism--one on ability and chronological age and the other on chronological age alone, being within the normal range of ability. Laboratory analysis of their urine samples was carried out blind as to the clinical diagnosis. RESULTS: The analysis correctly identified 53% of the autism group as against misidentifying 33% and 18% of the other two groups. When children with a severe learning disability (both with and without autism) were excluded from the comparisons, the laboratory then identified 77% of the 13 boys left in the autism group and misidentified 8% and 18% of the other two groups. CONCLUSIONS: The results would support the idea of a biological marker in prepubertal children and that it may be absent in, or obscured by the presence of severe LD.

Sexual abuse in children and adolescents with intellectual disability.

The present authors conducted a study of the occurrence of victimization and the perpetration of sexual abuse among 43 in-patients with intellectual disability aged between 9 and 21 years who were admitted to a child and adolescent psychiatric in-patient department over a period of 5 years. A retrospective case-note review was employed that explored the nature and severity of abuse in relation to the age, gender and level of disability. The prevalence of abuse or abusive behaviour, i.e. 14% of 300 admissions, did not change over time. In 13 out of the 43 cases, the issue of sexual abuse was identified after admission. Victimization alone occurred in 21 cases, perpetration alone in six cases, and both victimization and perpetration in 16 cases. Fifty per cent of the victims had been abused by a member of their close or extended family. Most cases (62%) were adolescents. There was only one instance of a victim being abused by a female. However, there were five girls who were perpetrators, all of whom had previously been victims. By contrast, 11 out of the 17 male perpetrators had been victims. Despite difficulties of disclosure, it was possible to establish that severely disabled patients had suffered sexual abuse. The present data support theories which (1) recognize gender differences in sexual abuse patterns and (2) have a developmental perspective, incorporating the influence of adolescence.

Psychopathology of sexual abuse in young people with intellectual disability.

The present study addressed two issues using a sample of child and adolescent victims and perpetrators of sexual abuse: (1) the extent of post-traumatic stress disorder (PTSD) in the sample; and (2) the possible distinction between perpetrators whose motivations were sexually impulsive, and those who were controlling and abuse-reactive. Retrospective case material from 43 cases (21 victims only, and 22 perpetrators, of whom 16 were also victims) provided the data. Post-traumatic symptomatology was not common. Only one case of PTSD was found. Perpetrators could be distinguished by whether they had suffered sexual abuse alone, sexual and physical abuse, or neither. The proposed distinction between perpetrators received support. Sexual abuse directed at younger victims was associated with earlier experience of multiple forms of abuse. The present data does not support the view that post-traumatic symptoms following victimization are a mediator of sexual abuse perpetration. It is argued that an elaboration of the Williams & New developmental model of perpetration better fits the data.

Screening for cervical abnormalities in women with anogenital warts in an STD clinic: an inappropriate use of colposcopy.

An audit of the use of colposcopy in women with anogenital warts was performed. Fifty women attending a clinic for sexually transmitted diseases in a District General Hospital with anogenital warts were examined by cervical cytology and colposcopy for cervical infection by human papillomavirus (HPV) or epithelial abnormality indicating cervical intraepithelial neoplasia (CIN) or both. Collated results showed a high prevalence of both conditions in these 50 women; 20 (40%) had evidence of cervical infection by HPV and 11 (22%) epithelial abnormalities consistent with CIN 1 or 2. However, neither CIN 3 nor invasive disease was detected. Colposcopy in this setting was shown to be a specific but insensitive tool and its role in the routine management of women with anogenital warts at our institution is not warranted.

Hypertension-accelerated atherogenesis in cholesterol-fed rabbits.

Entry of 125I-labelled low density lipoprotein ([125I]LDL) into the aortic intima was studied over 6 hours in normotenisve and hypertensive rabbits fed a 1% cholesterol diet for 9 and 4 weeks respectively. Studies were also made in hypertensive and normotensive cholesterol-fed rabbits in which blood pressure was reduced acutely with parenteral hydralazine. In all groups the entry of E1125I]LDL was greatest in the aortic arch and significantly less in both the descending thoracic and abdominal regions. Lipoprotein entry into the aorta of cholesterol-fed rabbits was increased some 10-fold over the corresponding value previously found in rabbits fed a normal diet [1]. This increase was due to increased vascular permeability as well as to increased plasma LDL concentration. The hypertensive cholesterol-fed rabbits did not show significantly greater entry of [125I]LDL than the normotensive cholesterol-fed rabbits. Comparison of the rate of LDL entry over 6 house and the quanitity of cholesterol accumulated in the aortic segments over the period of cholesterol feeding indicated that lipoprotein fractions other than LDL must contribute singificant amounts of cholesterol to the developing lesion. The finding that LDL entry paralledled accumulation during cholesterol feeding, together with the finding that acute reversal of hypertension did not reduce the entry of [125I] LDL suggest that mechanisms other than increased filtration of plasma low density lipoprotein contribute significantly to the accelerated development of atherosclerosis in hypertension.

Effect of hypertension on the in vitro incorporation of [1-14C]-oleate into phospholipid and cholesterol ester in the aortae of normal-fed and cholesterol-fed rabbits.

The effect of prior hypertension on the in vitro incorporation of [1-14C]-oleate into phospholipid and cholesterol ester in aortae from cholesterol-fed and normal fed rabbits was studied. Incorporation of [1-14C]-oleate into phospholipid was not increased in aortae from either hypertensive normal-fed or hypertensive cholesterol-fed rabbits when compared to the appropriate normotensive controls. In the normal-fed rabbits, incorporation of [1-14C]-oleate into cholesterol ester was increased by hypertension in all aortic regions. In cholesterol-fed rabbits cholesterol esterification was found to be proportional to the intimal cholesterol concentration, irrespective of the prior blood pressure or the particular aortic region studied. It is concluded that the increased lipid synthesis in atherosclerotic vessels from hypertensive rabbits is a consequence of the increased lipid accumulation produced by hypertension and not the result of hypertension directly stimulating arterial wall metabolism.

Incorporation in vitro of 14C-labelled acetate and 32P-labelled phosphate into lipid in thoracic aortae from hypertensive and nomotensive rabbits.

The effect of prior hypertension on lipid synthesis in the thoracic aortae of normal-fed and cholesterol-fed rabbits was studied in vitro using[1(-14)C] acetate and [32P] phosphate as lipid precursors. In normally fed rabbits, prior hypertension did not increase the incorporation of the labelled precursors into either phospholipid or neutral lipid. In cholesterol-fed rabbits, hypertension increased the incorporation of [32P] phosphate into phosphatidyl-choline and of [1(-14)C-acetate into cholesterol ester. The increased incorporation of [1(-14)C] acetate into cholesterol ester was accompanied by an increase in intimal total cholesterol concentration. For both normotensive and hypertensive cholesterol-fed rabbits there was a close correlation between cholesterol esterification and total cholesterol concentration of the thoracic intima. It is concluded that the increase in aortic lipid synthesis in hypertensive cholesterol-fed rabbits is secondary to the increased cholesterol accumulation induced by hypertension rather than to a direct stimulation of arterial wall lipid synthesis by hypertension per se.

Effect of hypertension on the entry of 125 I-labelled low density lipoprotein into the aortic intima in normal-fed rabbits.

The entry of [125I]-labelled low density lipoprotein (LDL) into different regions of the aortic intima has been studied over a 6 hour period in both normotensive and renal hypertensive rabbits fed a normal diet. Studies have also been carried out in previously hypertensive rabbits in which the blood pressure was normalized with parenteral hydralazine during the six hour period, in which entry was studied. In the normotensive rabbits entry into the aortic intima was less than 1 mug of LDL protein/100 mg dry defatted weight over the 6 hour period with greatest entry into aortic arch intima and significantly less into both the thoracic and abdominal aortic intimae. Hypertension increased the entry into the arch and into aortic arch intimae. Hypertension increased the entry into the arch and into the thoracic and abdominal segments but this was only statistically significant for the aortic arch. The entry of [125I] LDL into the intima in those rabbits in which the hypertension had been normalized was similar to that for the hypertensive rabbits. The results suggest that hypertension in the normal fed rabbit increases lipoprotein entry into the arterial wall by an effect on vessel wall permeability rather than by a direct effect of filtration pressure.

The effect of renal hypertension on the regional deposition of cholesterol and phospholipid in the aorta of normally- and cholesterol-fed rabbits.

The effect of renal hypertension on dry defatted tissue mass and lipid accumulation in different segments of the aortic intima was studied in both normally-fed and cholesterol-fed rabbits. In normally-fed rabbits hypertension caused an increase in intimal dry weight in the aorta. The increase was greatest in the lower thoracic intimal segment but was not significant in the aortic arch. The increase in tissue mass was not influenced by the addition of cholesterol to the diet and no regression of the increased tissue mass occurred when a 4-week period of hypertension was followed by a 4-week period of normotension. Hypertension did not increase the intimal cholesterol or phospholipid concentrations in normally-fed rabbits, suggesting that an observed increase in lipid content represented the cellular component of the intimal hypertrophy. Hypertension in cholesterol-fed animals caused preferential lipid accumulation in the lower thoracic segment, an effect that was independent of the total intimal cholesterol level. Intimal cholesterol, cholesterol ester and phospholipid were all increased. When a 4-week period of normotension and cholesterol feeding was preceded by a 4-week period of hypertension with normal feeding the amount of cholesterol deposited did not exceed that of the normotensive control, suggesting either that hypertension increased intimal permeability to lipid only in the presence of hypercholesterolaemia, or that healing of damaged intima had occurred before hypercholesterolaemia was fully established.